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Biomechanical Explanation/Advice needed

Discussion in 'Biomechanics, Sports and Foot orthoses' started by footphysio, Aug 10, 2008.

  1. footphysio

    footphysio Member

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    I have a few questions about some observations I have made with patients lately, that are different from the more "typical"patients I have seen in the past. I would like to know the mechanics behind these findings and orthotic advice.

    First, I have a very heavy lady with complaints of patella-femoral pain and planter fasciitis/cramping arches. Her shoes show severe lateral wear of the sole and the upper of the shoe is significantly deviated leterally. In standing, she has forefoot adductus (L) , low MLA (R>L), R varus calcaneus, L vertical, forefoot valgus bilaterally and has a medialy deviated STJ (R>L). What do you make of that?

    Second, I have another lady with longstanding plantar fasciitis. She was a little difficult to assess in standing due to significant pain. But, she appeared to have bilateral verticle heel and moderate arch height in standing (possibly varus heel, but was actively supporting). She had hypermobile TCJ dorsiflexion bilat., flexible forefoot valgus bilat. plus hypermobility through fore and mid foot. When her pain improved (through treatment by myself) her gait showed hyperpronation at midstance. RCSP showed 3degree varus on R, neutral L. NCSP showed 6 degree valgus on R, 4 degree valgus on L. Medially deviated STJ R>L.

    Some biomechanical explanation and orthotic advice would be appreciated.

    Thanks in advance.
  2. Not really enough information on this case but here's a hypothetical:
    Lots of lateral shoe wear + fat + medial STJ axis = big pronation moment = lots of stress on supinator tissues e.g. plantar fascia= plantar fasciitis. Low arch also may =abductor hallucis fatigue. Much pronation moment may well = lots of internal tibial rotation, if restriction of internal rotation at hip= "train wreck" at knee, maltracking = wear= chondromalacia

    A tale of interest: I saw a female runner last year who in static stance had really flat feet, I mean pes pancake, and really medial STJ axis. She had peroneal tendonitis:eek:. During running gait- marked forefoot lateral strike, no heel contact and laterally unstable- I forefoot valgus posted and got the outcome she was looking for. Moral of this tale: treat the tissue under stress by reducing mechanical load on that tissue, not the foot posture or wear on her shoes.:drinks Patients don't usually present with a fully or partially compensated rearfoot varus, they usually present with pain. Moral part 2: It is the dynamic function and dynamic excursion of the stj axis that is key (Spooner S.K., Kirby, K.A.: The Subtalar Joint Axis Locator. A Preliminary Report. Journal of the American Podiatric Medical Association. Volume 96 Number 3 212-219 2006). What does her gait look like?
    Last edited: Aug 11, 2008
  3. Craig Payne

    Craig Payne Moderator

    A temporary (ie FnHL) or permament (ie HR) increase in first MPJ stifness can cause this (ie the body moves laterally around the increase in stiffness (I really getting use to this new lingo!).
    ? low supination resistance? (STJ axis position only explains about a third of the force needed to supinate foot).
  4. Adrian Misseri

    Adrian Misseri Active Member

    Interesting morals, certainly simulating thoughts. However, if one reduces the mechanical stress to the tissues without correcting other aetological factors, is this not predisposing the tissue to reinjury?
    Last edited by a moderator: Aug 13, 2008
  5. footphysio

    footphysio Member

    What, in your opinion, is the other two thirds?

    I agree with both. Is the tissue not likely under stress due to the etological factors which causes the foot posture, shoe wear and pain? Don't you have to know the biomechanics of gait with say a rearfoot varus to know how to treat the foot properly?
  6. Craig Payne

    Craig Payne Moderator

    Bodyweight explains about a third and transverse plane position of STJ axis explains about a third; no idea what explains the rest (see this ref); BUT its NOT foot posture or alignment.
    Nope. Foot posture dosen't cause tissue stress.
    I never take into account rearfoot varus - its all about the forces behind the gait, function and foot posture.
  7. If we take a tissue stress approach to tissue injury and if through our intervention we reduce the stress in the injured tissue, how is this not addressing the aetiology? Perhaps you could explain Adrian?
  8. Adrian Misseri

    Adrian Misseri Active Member

    Cheers Simon,

    To reduce stress to a tisue is easy. In these cases, get the patinet off their feet for two weeks, thorugh bedrest, camm walkers, crutches, NWB ect. the stress on the tissue will be eliminated and the symptoms will resolve. However, if the underlying physiogical proceses are not addresed, such as pathomechanical foot function and excessive GRFs due to excessive bodyweight, the foot is predisposed to redirecting these excessive pathological forces back towards injury through the same pathways that caused injury in the first instance.


  9. Adrian, I didn't ask your opinion of how difficult it is to reduce tissue stress nor of the modalities available to achieve this objective. I asked you to provide support and explanation for your conjecture that "if one reduces the mechanical stress to the tissues without correcting other aetological factors, it shall predispose the tissue to re-injury". I don't believe that you have achieved this with you response.

    Given that we were talking about mechanically induced foot pain, perhaps you could provide a list of aetiological factors for this kind of tissue injury that do not increase tissue stress or mechanical load on the tissue? Since it is clear from your postings so far that you obviously don't believe that by using foot orthoses to alter the kinetics in a favourable manner resulting in a complete resolution of symptoms and allowing the said patient in the example I gave to go on to set a personal best time at the London Marathon was sufficient. The foot orthoses I prescribe aim to alter kinetics and reduce mechanical load on the target tissue. Tissue stress theory dictates that excessive mechanical load on the tissue caused the injury in the first place. Ergo, excessive mechanical load is THE aetiology. So if I've now changed the loading of the tissue through the use of foot orthoses, how can your statement that "the foot is predisposed to redirecting these excessive pathological forces back towards injury through the same pathways that caused injury in the first instance" hold true? How do your foot orthoses work, Adrian?

    To re-iterate my previous question, can you explain how altering forces in a favourable manner and allowing tissue healing is not, in your opinion, addressing the aetiology (cause) of mechanically induced foot pain? What causes mechanically induced foot pain Adrian? Put another way, how is "pathomechanical foot function and excessive GRFs due to excessive bodyweight" not addressed by my statement: "treat the tissue under stress by reducing mechanical load on that tissue"? Moreover, your responses thus far seem to imply that you believe these factors that you list do not add to the mechanical stress of the tissue since you initially said:

    Then you give as examples:
    If you address these factors what happens to mechanical stress in the tissues?

    Perhaps you could define the "physiological processes" of "pathomechanical foot function" for me, to allow me to understand the physiology of mechanics?
    Last edited: Aug 13, 2008
  10. R.E.G

    R.E.G Active Member

    Hi Simon,

    This has absolutely nothing to do with this thread, but I have failed to understand the new Pod Arena format :boohoo:

    Today I saw a young man from Rome (Italy).

    He presented with what turned out to be a bacterial infection of his fore foot, the point of entry seeming to be a deep callus that had resulted from scar tissue from previous surgical treatment to the plantar surface of his foot.

    In short I have never seen such a mess!

    I debrided the 'callus resulting in release of copious quantities of cream coloured pus.

    While waiting for this to drain we discussed Italy and Podiatry and he did nor seem to think that the speciality existed.

    My biomechanics is not bad but I defer to people like you in 'difficult cases'. However on a very superficial examination he had about 5degrees of pronation around neutral (please do not criticise my phraseology) and 70 degrees of supination.

    My guess was he was born with 'club foot' The history taking was intermittent, remember he booked in for the forefoot pain.

    The scar tissue on the plantar surface was a result of 'nodule operations' and he remembers significant 'physio' input as a child.

    End position do any of you know of 'Podiatry' in Italy?

    Any help is appreciated as I will only see him once more before he returns home.

    Bob Golding
  11. Bob,

    When was the surgery performed? If recent I'd send him back to the surgeon! Don't know specifically of any podiatrists in Italy other than Brian Rothbart. I know Brian reads this site so maybe he can help.
  12. R.E.G

    R.E.G Active Member


    as i said the history taking was far from ideal.

    The surgery was for 'cartilaginous growths' not too sure how long ago but would suspect over 10 years, sounds like the foot version of Dupetrans to me, but again 30 mins in a seaside practise?

    Yes I did find Dr R on a google search but no disrespect I was looking for a more English type top performing Pod.

    Seems in Italy his 'skin problems' would be treated by a dermatologist and his gait abnormalities by some form of Physio, but not the joined up concept Podiatry would provide. He for some reason thought he had verruca?

    He does also have Spanish connections.

    Made me think. I love Italian food so may well sell up and move to Italy?

    Any more help would be appreciated and more than happy to have a PM.

    Thanks Bob .
  13. Bob,
    Plantar fibromatosis is the foot version of dupuytren's- google it! ~It's possible that if this guy had club foot then some sort of soft tissue (plantar fascial) release may have been performed which could have lead to this. The nodules can be surgically removed but often re-occur. Treat the infection- antibiotics if necessary, heal the wound & off-load the problematic areas. I have had previous successes with plantar fibromatosis by employing softer orthoses (for example, laminates of eva, poron and plastazoate) with dells to off-load the nodules and plantar fascial grooves.

    Try Javier Pascual- podiatric surgeon in Madrid and member of this forum. VERY talented podiatrist.
  14. Adrian Misseri

    Adrian Misseri Active Member

    Sorry Simon for any offence that may have been recieved, none was, or has ever been, intended I assure you. Just trying to get my head around things and think out loud. My apologies. Just asking questions in an effort to learn.

    The idea I was trying to conceptualise is that the mechanical stress to tissues has to come from the foot being unable to cope with forces going through it. As an example, plantar fasciitis is due to mechanical stress to the plantar fascia, which will be reduced by an apporpriate orthotic. To that I have no argument. However to look at the relationship between the plantar fascia and the orthotic device directly, one could argue that the device is pressing on the plantar fascia from the plantar surface, and potentially adding different forces to the plantar fascia (be they causing mechanical stress or not). My argument is that the orthotic is controlling abnormal foot mechanics in the foot primarily, thus reducing the mechanical stresses to the plantar fascia as a secondary function.

    Take for example plantar fasciitis due to a failure of the windless mechanics due to excessive frontal plane motion at the midtarsal joint. The orthotic device reduces the excessive frontal plane motion at the midtarsal joint, thus allowing more 'normal' first ray plantar flexion at the metatarsal head, thus allowing more 'normal' hallux dorsiflexion, thus more 'normal' windlass function, thus less mechanical stress to the plantar fascia.

    I guess I'm suggesting that the mechanical stress is due to some part of the foot (and gait cycle) not doing what it's supposed to, and that the orthotic aims to correct this abnormal motion thus reducng the mechanical stress?

    Hopefully this helps me to explain myself. Thanks for all you assistance on this forum.
  15. Cheer up Adrian,

    I'm not offended by you. I am confused by your statements. What I think you are basically arguing is the old kinetics versus kinematics or force versus motion. That is, you believe the abnormal or pathological forces are the result of poor foot posture and motion and that to "treat" the resultant pathology one should attempt to alter foot posture and motion using the orthoses- right? Unfortunately orthoses don't always alter foot posture or motion, yet still work. This may be due to placebo, but also due to the fact that we can alter kinetics without altering observable kinematics. And this alteration in force is all we need to do to reduce mechanical stress in the tissue. This is my point.

    The argument I am making then is that ultimately it's not the motion nor the foot posture that cause pathology, rather it is the force on the tissue- agreed? Orthoses do not have to alter kinematics in order to reduce the force on a tissue. A good example of this is sinus tarsi syndrome in the maximally pronated foot. If we think of the STJ as a see-saw: if I put a fat kid on one end, the see-saw will move until the end with the fat kid on it hits the ground. In other words, we have both kinetic and kinematic change by adding the first fat kid to the see-saw. Now lets add another fat kid to the see-saw on the same end as fatty number 1. The see-saw will not move any further no matter how many fatties I add, but the compression force between the see-saw and the floor keeps increasing the more weight I add in. In other words, we have kinetic change without kinematic change. Lets add half a dozen bloaters to the same end of the see-saw. Now lets put a small baby on the other end of the see-saw (or better in terms of the orthosis analogy, get him/ her to try and pull on the fat kids end of the see-saw). Again we aren't going to see any change in position of the see-saw, but the compression force between the ground and the see-saw and the internal stresses within the see-saw will have changed. Back to sinus tarsi syndrome, lets say we know in our patient the pain they are experiencing is due to compression between the calcaneus and talus at the floor of the sinus tarsi, our orthosis doesn't need to change the position of the STJ to resolve the symptoms, merely to lower the compression force (residual pronation moment) at the floor of the sinus tarsi. Thus, we only need kinetic change not kinematic change, because it is the force not necessarily the position which is causing the problem. Hope this makes sense.
    Last edited: Aug 14, 2008
  16. Adrian Misseri

    Adrian Misseri Active Member

    Thanks for the explanation Simon, and you're right, I do tend to see the kinetics vs kinematics idea as more tangable in my head at times, essentially abnormal pathological forces have to come from somewhere, and that would have to be from some part of the foot not doing what it should to deal with those forces. Your use of fat kids has helped explain the tissue stress idea for me, and nice way to get fat kids outside on play equipment instead of inside!

    Would it be a fair comment to suggest that it is the time over which the force is applied (essentially the 'impulse' to coin a physics term) which is a major contributing athological factor, and although an orthotic device may not nesessarily alter a foot shape, but it may reduce the time over which the forces act (reduce the impulse)?

    Sorry footphysio tha this thread has gone sooooo far off topic, but I'm learing from it!

  17. footphysio

    footphysio Member

    Well, my question generated a lot more discussion than I anticipated. But, I am glad. My question now seems irrelevent. I must admit I haven't totally grasped the idea of looking at kinetics rather than kinematics. Therefore to drill the points further into my head :hammer:I have to ask some questions that I know have been answered over and over again (Thanks Simon and Craig!). Here it goes!

    So foot posture (i.e. forefoot/rearfoot var/val) doesn't contribute to overpronation, underpronation, deformities etc. and therby injury?

    Has the "old way" of assessing the foot by measuring angles etc. has been thrown out the window?

    What do you look at in an foot assessment ? (I believe there is a previous post regarding this somewhere - I can look that up if it has been covered already)

    How do you take measurements of the forces that are causing tissue stress? How do you know how much stress relief will be enough to let the tissue function without damage? ( did that question make sense? - couldn't word it quite right). Further to that, how then do you determine the amount of post/skive/inversion to prescribe in an orthotic ?

    That should be enough questions for this post :dizzy:. Thanks again for sharing your knowledge.
  18. Simon has very nicely provided an analysis of the tissue stress theory of mechanical foot therapy. The key points of the tissue stress theory of mechanical foot therapy is that the clinician should first identify the anatomical structure that is the cause of the pain/pathology, then determine the structural/functional factors that are the cause of the pain/pathology, and finally design a treatment plan that will reduce the pathological stresses on the injured tissue and will improve gait dynamics, without causing other injuries/symptoms.

    One cannot separate kinetics from kinematics in biomechanics. Changes in kinetics cause a change in kinematic function. Therefore, if one identifies a change in kinematic function, then one also knows that the kinetics has changed. However, if there is no change in kinematic function, one can not also presume that there is no change in kinetics, since, as Simon notes, the internal forces and internal moments may have changed with no apparent change in joint position.

    In addition to the see-saw example that Simon provided and is outlined in two of my papers (Kirby KA: Rotational equilibrium across the subtalar joint axis. JAPMA, 79: 1-14, 1989; Kirby KA: Subtalar joint axis location and rotational equilibrium theory of foot function. JAPMA, 91:465-488, 2001), one can simply think of what happens internally within a wall of your home when you push against it. We know that the external forces have changed on the exterior of the wall, since you are now pushing on it. From Newton's laws, we also know that the internal forces and moments within the wall must have changed, since the wall has not moved in response to the external pushing force. However, since the wall has not moved, then the kinematics of the wall has not changed but the kinetics has. This is another example I commonly use in my lectures to explain how orthosis may work to heal mechanical injury without altering the motion of the foot and/or lower extremity.
  19. Impulse is important, but so too are all the other properties of a force.
  20. I had a good teacher.:drinks
  21. Foot posture contributes to and is a consequence of the forces within and applied to the foot. Overpronation, whatever that is, is not the problem, to paraphrase Eric Fuller, it's the deceleration of that motion that causes the problem.

    I guess it depends on who you are talking to and what you are doing with angles.

    Many things, but ultimately as Kevin has stated, it's about identifying the tissue under stress and understanding the functional role of that tissue in running, walking, hoping, jumping- whatever it is that is leading to the problem.

    For research purposes we use inverse dynamics. But clinically you don't really have to. If you can identify the tissue under stress and if you understand the forces that would place that tissue under stress, have an appreciation of how orthoses prescription variables can be used to manipulate forces beneath the foot, then you know that by reducing those "pathological" forces using you orthotic knowledge the tissue will be under less stress.

    A great question, the best to be asked in this thread and one that I've asked of my mentors many, many times. Kevin- why 15 degrees? Once more!!!! The reality is that you don't know exactly, you use educated guesses and clinical experience most of the time. Certain tests may help, but ultimately its a guess. Angles are an artifact from previous paradigms, it's all about how much force to apply and where and when. We are much like children only just beginning to understand this.

    In the future we will use modelling to solve these problems but for now we use educated guesses in the main.
  22. footphysio

    footphysio Member

    Once again, Thanks for all the information given in this thread and all the others in this forum. It really is appreciated that you have shared your knowledge and take the time to answer repeated questions.

    I have read, but cannot quote directly at this time, that to make a one degree change of inversion of the foot one must invert the orthotic 5 degrees. Is this something that is widely accepted?
  23. No! I know where that number comes from and it is simply not true. It is a guess and should not be accepted as fact. See the thread on supination resistance and my papers on rotational equilibrium across the STJ axis and you will better understand why it simply is not true.
  24. efuller

    efuller MVP

    Well answered Simon.

    My original quote that simon paraphrased is it's not the pronation that hurts, it's the stopping of pronation that hurts. Simon's paraphrasing is better in that you can see Newton's second law in his sentence. However, those who are not familiar with Newton's laws may not get the reference.

    As was mentioned already, you identify the injured structure. The old angle measurements often did not make a good connection between the injured structure and the measurements. A rearfoot Varus causes 1st MPJ pathology????? Everyone (> 95%) has a rearfoot varus and not everyone has 1st MPJ pathology.

    One important thing to look at in foot assessment is STJ axis position in the transverse plane. This is critical because this and the location of center of pressure under the foot determine the moment from ground reaction force about the STJ axis.

    You cannot always model your treatment based on the idea that the tissue that hurts is damaged by STJ pronation therefore I must increase supination with my treatment. Some of the people who exhibit late stance phase pronation have a lateral deviated STJ axis (over supinated) foot. It is my belief that these individuals pronate in late stance because they use their muscles to pronate their STJ at this time in gait. Doing this prevents ankle sprains. So, you still have to understand why the foot pronates. Is it pronation caused by the ground or pronation caused by the muscles? You would treat them differently. This is actually one of the successes of the angular measurement paradigm. Late stance phase pronators often had a forefoot valgus and recieved forefoot valgus wedging in their devices and their symptoms improved. If you really want to make your head hurt try and use the old paradigm to explain why a forefoot valgus wege should decrease pronation.

    The angle measurements have not been discarded by all. You are in the middle of a paradigm shift. Some folks are still in the old paradigm and some in the new.


    Eric Fuller
  25. footphysio

    footphysio Member

    What are the indication for medial skive vs. inversion vs. both together?
  26. Craig Payne

    Craig Payne Moderator

    The greater the force needed from the orthotic (~supination resistance force), the greater the wedging/inversion/skiving of the rearfoot (probably dosen't matter which one).
  27. Admin2

    Admin2 Administrator Staff Member

  28. When the positive cast is balanced inverted, there is significant raising of the medial longitudinal arch (MLA) height of the orthosis, with minimal change in the plantar heel cup contour of the orthosis, especially if the plantar heel cup contour of the foot is rounded and not flat. When a medial heel skive modification is used (Kirby KA: The medial heel skive technique: improving pronation control in foot orthoses. JAPMA, 82: 177-188, 1992.), the positive is cast is modified so that there is an additional varus plantar heel cup shape added to the resultant orthosis.

    When I am using a medial heel skive, I will always invert the positive cast between 2-8 degrees in order to also increase the MLA height of the resultant orthosis in order to benefit from the synergistic "anti-pronation effect" of having both the heel in varus and the MLA of the orthosis higher. Raising just the MLA of the orthosis by inverting the cast, without using a medial heel skive will tend to increase the risk of MLA irritation of the foot. Inverting the positive cast will also increase the varus forefoot correction (or decreased valgus forefoot correction) in the positive cast so that this may be either positive or negative for the patient depending on what you are trying to accomplish with the orthosis.

    The more you become familiar with how inverting the positive cast versus adding a medial heel skive specifically changes the shape of the resultant foot orthosis, then you will tend to use more of one or another as the biomechanical needs of the patient dictate. They are definitely not the same mechanically but I tend to use them together often in different combinations depending on the patient's needs.

    Hope this helps.
  29. I still do measurements in addition to other tests that I find quite helpful. I like being able to assess the basic structure of the foot and lower extremity and compare it to other feet I have seen. Doing measurements is very helpful for me to get a better sense of a patients' structure compared to other patients' structure. If you haven't done the measurements, then you really don't know what you are missing.

    There is recent research coming out of UC Davis biomechanics lab that I am reviewing for a master's research project which shows positive correlation between some biomechanical measurements and foot and lower extremity kinematics and kinetics during running. I think that, in the future, we will see much more research showing some correlation of kinetics to structural variation. Therefore, my advice is to not give up on taking measurements....we definitely haven't heard the last word on this subject yet.
  30. Mark Denman

    Mark Denman Welcome New Poster


    Hi, my name is Mark and I'm a uni student at QUT in Brisbane, Australia and was hoping to ask a question about your first post.

    What did you mean by "foot posture"? I generally think of this term very broadly but most importantly as the posture and function of my specific patient's foot.

    I ask this with reference to your "pes pancake" patient

    "A tale of interest: I saw a female runner last year who in static stance had really flat feet, I mean pes pancake, and really medial STJ axis. She had peroneal tendonitis:eek:. During running gait- marked forefoot lateral strike, no heel contact and laterally unstable- I forefoot valgus posted and got the outcome she was looking for. Moral of this tale: treat the tissue under stress by reducing mechanical load on that tissue, not the foot posture or wear on her shoes."

    I had an almost identical patient in our clinic, only differences/additional info being
    • she didn't do much running (was a swimmer)
    • had a flexible forefoot valgus

    I treated her in an identical fashion becuase I wanted to reduce the load on her peroneals, but did so because I was of the opinion that her Peroneals were overloaded because:-
    Her FFVL would supinate the FF when loaded, unlocking the MTJ locking mechanism at Calc-cuboid joint (thus requiring peroneal contraction to provide pressure on the MTJ (CC) joint to achieve a rigid'ish foot for propulsion (i.e. achieve close-packed lateral column). I felt this was why she adapted her running style to laterally load the FF.

    In this regard I thought FF valgus posting would assist in locking the MTJ allowing for more efficient use of osseous structures and would reduce the mechanical load placed on muscles that cross this joint.

    In this regard I consider "foot posture" to be a term for a patient's individual feet, not a hypothetical "normal", but consider it very relevant to determine how the load is placed on the tissue under stress and how it can be reduced. (i.e. any muscle is simply a pulley that crosses a joint, attaches to the two bones in question and moves said bones by applying force. In considering how to reduce the load you have to investigate the arrangement/posture of the structures.)

    So 2 Q's:-
    (1) by considering foot posture/ function in the way I have "am I barking up the wrong tree?"
    (2) in your own experience treating your patient above, I would have thought the use of valgus posting could be described an intervention in "foot posture" - albeit with a specific functional impact in mind that would reduce the load on the oveloaded muscles/tendons, rather than some hypothetical "normal/optimum" foot posture?

    I guess I really wanted to clarify what you were communicating as I think this may have thrown Adrian in his earlier post.

    Thanks in advance as any guidance is greatly appreciated.

  31. Foot posture is the position of the tissues of the foot.

    Firstly, there is no such thing as an MTJ locking mechanism. Why can't the metatarsals dorsiflex at their proximal articulations with the cuneiforms to compensate for the flexible forefoot valgus? Probably a whole new thread, but at the time during the gait cycle when "compensation" for a flexible forefoot valgus should occur and given the forces acting across the talonavicular and calcaneocuboid joints at this time in this foot type, what is the resultant orientation of the MTJ axis likely to be? What other theoretical mechanisms could explain the lateral forefoot propulsive strategy?

    Please re-read my posts in this thread, I have not said foot posture is not important.

    You assume your intervention has changed the kinematics, it may or may not have. The point is, you don't need to. Please re-read the posts in this thread.

    Adrian seemed to be suggesting that there were additional aetiological factors other than those which contribute to the stress in the dysfunctional tissue and that these must be addressed to prevent reoccurrence of the tissue dysfunction; I'm still trying to work out what these are. Perhaps you could help me out?
    Last edited: Aug 19, 2008
  32. Mark Denman

    Mark Denman Welcome New Poster


    Thanks for your help and please forgive me if I'm "off the pace" with my biomechanical knowledge.

    I think we may have been on the same page but I will admit I found it hard to articulate what I was saying on-line. After a re-read I found another quote by yourself that says it well:-

    "For research purposes we use inverse dynamics. But clinically you don't really have to. If you can identify the tissue under stress and if you understand the forces that would place that tissue under stress, have an appreciation of how orthoses prescription variables can be used to manipulate forces beneath the foot, then you know that by reducing those "pathological" forces using you orthotic knowledge the tissue will be under less stress. "

    I will admit you've now got me thinking about your comment that:-
    "Why can't the metatarsals dorsiflex at their proximal articulations with the cuneiforms to compensate for the flexible forefoot valgus? Probably a whole new thread"

    Could I ask a favour for a nudge in the right direction as to where there might be any good literature in this regard?

    As for Adrian's post I can't shed much light there as I found it a little confusing when I read the replies. I think that Adrian and yourself might have been at crossed purposes. Adrian seemed to speak of treating the tissue, as injured tissue i.e. Ice, rest etc, whilst I understood yourself to be talking about taking the mechanical load off the tissue?
    Sorry Adrian if it looks like I'm putting words in your mouth. (again still getting used to this on-line thing)

  33. Lundgren P, Nester C, Liu A, Arndt A, Jones R, Stacoff A, Wolf P, Lundberg A: Invasive in vivo measurement of rear-, mid- and forefoot motion during walking. Gait and Posture, 28:93-100, 2008
  34. Adrian Misseri

    Adrian Misseri Active Member

    G'day all,

    I've taken a couple of days to sit down and have a think about how to best explain what I was trying to get across in my earlier posts. :wacko:

    In a static foot (like the see-saw with the fat kids, and pressing on a wall), the forces which are acting on the tissues are in equilibrium as there is no motion. This is regardless of magnitude of the forces, and the only way in which the structures under load can fail under these forces is if the force on a particular structure exceeds the strength of the structure. i.e. the plantar fascia under tension and the force acting on it is greater than the strain coefficient (the see-saw will break if the fat kids weigh more than the see-saw can hold).

    However, the foot is not a static structure. For motion to occur, forces must be unbalanced. i.e. a ball rolls when it is pushed, and the pushing force overcomes the friction force of the ball on the ground. In a 'normal' foot with 'normal' forces acting through it through gait, the magnitude of the forces acting on the various soft tissues and osseous structures (including joints) are not excessive enough to overcome the strength of the structures. Mechanical strain then occurs on a structure in the foot which is being subject to forces with a magnitude greater than that of which the structure can withstand. To get these forces to the pathological magnitude required to cause strain, one or more of several things have to occur:
    1. Increased GRF due to bodyweight (the kids get fatter)
    2. Tissues (soft tissue, bone etc.) are weakened by pathology (the see-saw is faulty)
    3. Motion of the foot is beyond 'normal' motion (i.e. excessive pronation at the midtarsal joint, hallux limitus causing sagittal plane blockade etc.), and this leads to increased magnitude of forces to the structures (the see-saw is not moving properly)
    4. Anatomy of the foot is such that the foot is subject to excessive forces i.e. medially deviated subtalar joint axis, excessively long second metatarsal etc. (the see-saw doesn't move properly because it was made poorly)

    The use then of orthoses can then help with numbers 2, 3 and 4. It can help number 2 by redirecting and redistributing the forces and offloading the weakened structures (i.e. a rearfoot controlling device will take the strain off an injured posterior tibialis tendon by inverting the rearfoot). Number 3 is assisted as the abnormal motion of the foot can be corrected with orthoses (i.e. first ray cut out allowing plantarflexion of the 1st MTPJ and activation of the windlass mechanism). Number 4 is assisted by orthoses as the forces can be directed around the abnormal anatomy (i.e. a medial heel skive will add extra force to the medial side of the medially deviated subtalar joint axis to control the pronatory moment).

    My idea, therefore, is that orthoses change the forces by controlling motion in the feet, as it is the motion which leads to the excessive magnitude of forces which cause injury to the tissues, and the orthotic controls the forces in the motion.
    Hopefully this explains myself better? :sinking:

    Thanks for all your feedback everyone by the way!
  35. Craig Payne

    Craig Payne Moderator

    Its the other way round. Forces drive and stop the motion. Forces can be changed without having any effect on motion.
  36. DaVinci

    DaVinci Well-Known Member

    At a seminar in Melbnourne last week, CP explained and showed (with evidence) really well, how foot orthoses change forces and no not necessarily change motion, nor do they need to change the motion. It made a lot of sense. Adrian ... you really need to see the diagrams and pictures that CP uses in the way he explains it.
  37. Adrian Misseri

    Adrian Misseri Active Member

    Thanks Craig, I agree with that statement, makes sence and is logical:drinks.
    I'm just trying to undertand where the forces are coming from initally that are causing the stress to the tissues.
  38. Adrian and Colleagues:

    Adrian, I read over your above analysis and would agree with it for the most part. However, as Craig noted, to say that "orthoses change forces by controlling motion" is not an accurate statement. Orthoses alter the magnitudes, temporal patterns, and points of location of ground reaction force on the plantar foot. They don't always "control motion" or even alter motion (i.e. the motion we can detect with our current kinematic analysis methods). However, they do always alter the kinetics, or forces and moments acting with the foot and lower extremity and across the joint axes of the foot and lower extremity.

    Let's consider an example. A clinician and engineer are asked to analyze the mechanics of a brick wall in response to a pushing force from a 250 pound man. The man pushes hard against a brick wall and the clinician, given the task to assess whether the man has changed the mechanics of the brick wall, only measures whether the wall moves or not when the man has pushed against it. The clinician then concludes that the man has not changed the mechanics of the wall since the wall did not move. However, the engineer, when analyzing the same situation mechanically, deduces that due to Newton's Laws of Motion, that the brick wall had to be pushing against the man with the same force as the man pushed against the brick wall to achieve static equilibrium. In order to do so, the engineer confidently states that the internal stresses and internal strains of the components of the brick wall had to change in order to allow static equilbrium of the brick wall to be maintained, even when being pushed on by the 250 pound man. Therefore, the engineer concludes that the mechanics of the brick wall has changed by the man pushing on it.

    The real question then becomes.......which one so you think like.....the clinician or the engineer?? I prefer to be a clinician that thinks like an engineer since my patients benefit from this way of thinking.
    Last edited: Aug 23, 2008
  39. Craig Payne

    Craig Payne Moderator

    Imagine a foot that has pronated to end range of motion with bone on bone contact in the sinus tarsi and the compressive forces at this end ROM are high and are causing symptoms.

    Lets put an orthotic under this foot and assume that the sum of all the orthotic reaction forces (ORF) are medial to the STJ, so it has a lever arm, which means one of two things:
    1. The magnitude of that ORF are sufficent to move that foot away from end ROM
    2. The magnitude of that ORF are NOT sufficent to move that foot away from end ROM

    Both situations can result in symptom reduction:
    1. The STJ has been moved away from end ROM --> symptom reduction
    2. The ORF was not sufficient to move the foot away from end ROM, but as the sum of the ORF's is medial to the STJ (has a lever arm), there will have to be a mechanical effect at the other side of the pivot point (STJ axis) of the lever, so the STJ will still be an end ROM, but now the bone on bone contact force is minimal (the compressive forces are reduced) --> symptom reduction.

    In (1) we changed motion (kinematics) and force (kinetics).
    In (2) we just changed forces (kinetics).

    To achieve a reduction in symptoms, we only need to change the kinetics (ie the forces in the tissues).

    Williams & McLay et al showed on systematic differences in the kinematics between orthotics that worked and did not work; they showed massive systematic reductions in the kinetics for the orthotics that worked compared to the orthotics that did not work.
  40. efuller

    efuller MVP

    Hi Adrian,

    I agree with Kevin and Craig's posts. I thought I'd make a few comments to try and guide you a little more to the force not the position ideas. You have to examine your implied assumptions.

    I agree with 1 & 2. Bad collegen will cause problems.

    Let's look at point 3. What is motion beyond normal motion? What limits normal motion?

    We could consider the end of range of normal motion as the point at which ligamentous tension increases and limits motion. This is a generic term, because not all joints, in all positions, is motion limited by ligaments. Sometimes, as in the STJ, motion is limited by bone on bone contact. So, some of the time "excessive motion" will occur with stretching of the ligaments. In the case of late stance phase pronation of the STJ, I would maintain that the joint stops somewhere in the middle of its "normal" range of motion and the late stance phase pronation is within the "normal" range of motion.

    What hurts with sagittal plane blockade. You have to identify the strutcure in pain and then figure out how to alter the stress on that structure.

    Point 4 said another way. The anatomy of the foot is such that a particular anatomical structure will be stressed more than the average foot. e.g. long second metatarsal.

    The orthotic does not necessarily invert the rearfoot, but it does decrease the pronation moment from ground reaction force. The moment from ground reaction force can be reduced without seeing the foot actually supinate.

    When there is a dorsiflexion moment on the hallux (heel raise in gait) there is an attempt to activate the windlass. Whether or not the windlass moves depends on the forces and moments acting on and within the windlass. Increased force on the hallux and 1st metatarsal will create a dorsiflexion moment on the first ray. A dorsiflexion moment on the first ray will tend to increase tension in the fascia. Tension in the fascia will increase the plantar flexion moment acting on the proximal phalanx hence the toe will not dorsiflex. As the tension in the fascia is reduced, it will reach a point where the dorsiflexion moment from the ground will be greater than the plantar flexion moment from the fascia. At that point there will be acceleration in the direction of dorsiflexion.



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